Date of Award

2023

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Molecular Biology

Abstract

SELENOF is an understudied selenium-containing protein that has previously been postulated to behave as a tumor suppressor in the breast. Examination of patient databases showed that SELENOF levels were lowest in tumors from patients with aggressive late-stage breast cancers. Whether loss of SELENOF drives breast tumorigenesis remains to be determined. To address this question, we used juvenile female wild type or systemic Selenof knockout mice and exposed them to 7,12-Dimethylbenz[a]anthracene (DMBA), a carcinogen that replicates the multistep process of breast tumorigenesis. Previous reports have shown that loss of Selenof led to glucose and metabolic dysregulation in mice suggesting a link between Selenof and metabolism. Because obesity is a risk factor in breast cancer, we challenged the mice with a Western diet, high in fats and calories, to mimic obesity. We hypothesized that loss of Selenof would promote DMBA-induced tumorigenesis and the Western diet would exacerbate it. We found that overall tumor incidence was in fact highest in the Selenof knockout mice and Western diet group. However, mammary tumor incidence was equal between the Selenof knockout and wild type cohorts. The Selenof knockout mice did not exhibit higher weights, however, they did exhibit higher fasting glucose levels, consistent with metabolic dysfunction. These findings indicate that the link between SELENOF, obesity, and breast cancer warrants further investigation.

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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